Evidence map›Paper›PMID 28472257›Full record

ArticleJournal of Crohn's & colitis2017

Expression of Ecto-nucleoside Triphosphate Diphosphohydrolases-2 and -3 in the Enteric Nervous System Affects Inflammation in Experimental Colitis and Crohn's Disease.

Linda Feldbrügge, Alan C Moss, Eric U Yee, Eva Csizmadia, Shuji Mitsuhashi, Maria Serena Longhi, Bynvant Sandhu, Holger Stephan, Yan Wu, Adam S Cheifetz and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 24 citations in OpenAlex.

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  13. Ectonucleotidases in Inflammation, Immunity, and Cancer.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 3 countries.

Linda FeldbrüggeDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Alan C MossDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Eric U YeeDepartment of Pathology, OU Medical Center, Oklahoma City, USA.
Eva CsizmadiaDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Shuji MitsuhashiDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Maria Serena LonghiDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Bynvant SandhuDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Holger StephanHelmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Dresden, Germany.
Yan WuDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Adam S CheifetzDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Christa E MüllerPharmaceutical Institute, University of Bonn, Bonn, Germany.
Jean SévignyDépartement de Microbiologie-infectiologie et d'Immunologie, Université Laval, Québec, QC, Canada.
Simon C RobsonDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Z Gordon JiangDivision of Gastroenterology and Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USHelmholtz-Zentrum Dresden-Rossendorf · DEUniversité Laval · CAUniversity of Bonn · DEUniversity of Oklahoma Medical Center · US

Funding

Therapeutic assessment of synthetic heparin sulfates in transplantation modelsP01HL107152 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI BALAGURUNATHAN, KUBERAN · 2011 to 2017
$15.8M
Role of enteric glia in the death of neurons during gut inflammationR01DK103723 · NIDDK · MICHIGAN STATE UNIVERSITY · PI BRIAN D. GULBRANSEN · 2015 to 2026
$4.7M
Immunomodulatory effects of bilirubin are mediated through aryl hydrocarbon receptor, O2 and purinergic pathwaysR01DK108894 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LONGHI, MARIA SERENA · 2017 to 2021
$2.0M
Purinergic Pathways in Crohn's DiseaseK23DK084338 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MOSS, ALAN COLM · 2011 to 2015
$735k
Engineering Inhibitory Antibodies to Ectoenzymes for Cancer TreatmentR21CA164970 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2012 to 2013
$405k
NCI NIH HHS R21 CA164970NHLBI NIH HHS P01 HL107152NIDDK NIH HHS K23 DK084338NIDDK NIH HHS R01 DK103723NIDDK NIH HHS R01 DK108894
6 · The paper itself

Abstract

objectiveRecent studies have suggested that the enteric nervous system can modulate gut immunity. Ecto-nucleoside triphosphate diphosphohydrolases [E-NTPDases] regulate purinergic signalling by sequential phosphohydrolysis of pro-inflammatory extracellular adenosine 5'-triphosphate [ATP]. Herein, we test the hypothesis that E-NTPDases modulate gut inflammation via neuro-immune crosstalk.

designWe determined expression patterns of NTPDase2 and NTPDase3 in murine and human colon. Experimental colitis was induced by dextran sodium sulphate [DSS] in genetically engineered mice deficient in NTPDase2 or NTPDase3. We compared plasma adenosine diphosphatase [ADPase] activity from Crohn's patients and healthy controls, and linked the enzyme activity to Crohn's disease activity.

resultsNTPDase2 and -3 were chiefly expressed in cells of the enteric nervous system in both murine and human colon. When compared with wild type, DSS-induced colitis was exacerbated in Entpd2, and to a lesser extent, Entpd3 null mice as measured by disease activity score and histology, and marked anaemia was seen in both. Colonic macrophages isolated from Entpd2 null mice displayed a pro-inflammatory phenotype compared with wild type. In human plasma, Crohn's patients had decreases in ADPase activity when compared with healthy controls. The drop in ADPase activity was likely associated with changes in NTPDase2 and -3, as suggested by inhibitor studies, and were correlated with Crohn's disease activity.

conclusionsNTPDase2 and -3 are ecto-enzymes expressed in the enteric nervous system. Both enzymes confer protection against gut inflammation in experimental colitis and exhibit alterations in Crohn's disease. These observations suggest that purinergic signalling modulated by E-NTPDases governs neuro-immune interactions that are relevant in Crohn's disease.

Indexed as

Adenosine TriphosphatasesAdolescentAdultAnimalsApyraseBiomarkersCase-Control StudiesColitisColonCrohn DiseaseDextran SulfateEnteric Nervous SystemFemaleHumansMaleMiceAdenosine TriphosphatasesApyraseBiomarkersDextran SulfateectoATPaseCrohn’s diseaseectonucleotidaseenteric nervous system

Identifiers

PMID28472257
PMCPMC5881706
OpenAlexW2610241312

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.